Phospholipase A2 Group IIa was examined by polymerase chain reaction-based single strand conformation polymorphism and direct sequencing in 55 patients from 45 families with familial adenomatous polyposis.
Phospholipase A2 Group IIa was examined by polymerase chain reaction-based single strand conformation polymorphism and direct sequencing in 55 patients from 45 families with familial adenomatous polyposis.
PLAP was considered a potential candidate to be involved in malignant melanoma because it maps to the critical region for CMM and because the PLA2 gene has been identified as a modifier of the APC gene, responsible for the adenomatous polyposis phenotype in the mouse.
Overexpression of the nonpancreatic secretory group II PLA2 messenger RNA and protein in colorectal adenomas from familial adenomatous polyposis patients.
A modifying locus, called Mom-1, which strongly influences disease expression has been mapped in the mouse model of FAP to the region of murine chromosome 4, which has synteny to human chromosome 1p35-36.
Mutation of Pla2g2a, a secretory phospholipase A(2) gene, dramatically increases the number of intestinal polyps that develop in the multiple intestinal neoplasia (Min) mouse, a murine model for adenomatous polyposis coli in humans.
In the current study no inactivating mutations in the sPLA2 gene were identified, suggesting that human sPLA2 is not associated with phenotypic variation in FAP.